EMERGENCY ROLL OUT OF COVID-19 VACCINE, BUT WITH MILLIONS ALREADY WITH CIRCULATING ANTIBODIES ,FALL IN NEW CASES AND MORTALITY IN INDIA, IS IT AN EMERGENCY SITUATION ANYMORE?
After every vaccination in general body doesn’t remain the same as before as now it has some additional circulating antibodies which earlier were not being produced in body, this changes the whole complex dynamics of interaction beyween multiple systemic components of body and also the epigenome and genome. This may have immediated or delayed, slow and gradually developing complications which might not be evident initially for many years!
Vaccines needs to be time tested, there are not only immediate reactions but also long run late developing complications associated with vaccines which need to be evaluated for years before rolling it out in market.
In emergency situations they may skip certain regular protocols to release vaccine if Risk- to -Reward ratio is good.
Looking at current scenerio in India we are observing that most of the country is functioning almost at its pre-pandemic levels, still the cases have fallen and also the mortality rate is falling.
Reason being many of us have already developed immunity against COVID 19 and have circulating antibodies in our blood.
With time and subsequent chain of transmissions, also the virus mutates and may form many various strains. Few new mutated strains may be stronger and few may be milder for humans, these milder strains acts as a sheild or natural vaccine against many stronger strains. As individuals infected with these milder strains may not develop severe symptoms and develop antibodies which will drive immunity against many other stronger strains as well.
So when we see on-ground reality that the fresh infection cases are falling with reduced severity and mortality, we should re-think that wether now its required to emergency roll out vaccine now with fast declining cases and deaths in India.
Don’t we need to think again before emergency roll-out of COVID-19 vaccines for mass vaccination, in interest of health of masses, leaving aside the interests of big pharma giants, with falling cases wether its still an emergency situation in India!
And if still its evaluated an emergency situation then why not to make it mandatory to get antibody test done before vaccination, to exclude those who already have circulating antobodies and/or have past record of COVID-19 infection may not require the vaccine thus reducing unnecessary vaccinating many who actually dont require.
Just because the vaccine has been developed and billions of dollars and scientist hours are being invested doesn’t mean that we emergency roll out and vaccinate everyone at collosal scale even those who actually don’t require or are at risk of developing vaccine complications!
There are countries where the impact and severity is still high and pandemic is still causing havoc, for such countries definitely vaccines will prove saviour.
Pernicious Anaemia is caused due to deficiency of Vitamin B12.
Pernicious literally means deadly, if untreated patient may develop irreversible pathological changes also stomach cancer in many untreated long haulers. Untill adevent of Vitamin B12 treatment it was considered untreatable and fatal but now with proper regular vitamin B12 supplimentation it is easily treated.
CAUSES OF PERNICIOUS ANAEMIA
Pernicious Anaemia is a later stage complication of Vitamin B12 deficiency.
Vitamin B12 deficiency may be due to
Dietary insufficiency of Vitamin B12
Lack of Gastric Intrinsic Factor(GIF) due to various pathological factors that may damage Gastric Parietal Cells which produces Gastric Intrinsic Factor eg autoimmunity etc.
Other reasons like partial or complete gastrectomy.
Lack of Hepatocorin due to corresponding gene defect.
PATHOPHYSIOLOGY OF PERNICIOUS ANAEMIA
Transportation and Absorption of Vitamin B12
TCN1 gene on chromosome 11 is responsible for production of transcobalamine-1 also called as Heptacorrin which is a glycoprotein secreted by salivary glands binds with VitaminB12 to form Heptacorrin-VitaminB12 complex thus helping transport of acid-sensitive vitamin B12 safely through the acidic medium of stomach into the deudenum region of small intestine.
In deudenum, the proteases from pancreatic enzymes degrade and detach this glycoprotein carrier heptacorrin from Vitamin B12.
Vitamin B12 in then gets attached to Gastric Intrinsic Factor also called Intrinsic Factor. GIF gene on chromosome 11 is responsible for production of Gastric Intrinsic Factor which is a glycoprotein secreted by parietal cells of stomach.
After attaching to Gastric Intrinc Factor this GIF-VitaminB12 complex is then transported and absorbed by Enterocytes in ileum region of small intestine.
In ileum, the Gastric intrinsic factor is detached and degraded from this GIF-VitaminB12 and Vitamin B12 is relaeased. Vitamin B12 is then taken up by Transcobalamine-2 (TCN2) which is then transported to tissues.
Biochemical Role Of Vitamin B12
Vitamin B12 is required to synthesis 5-Methyltetrahydrofolate and Homocysteine in presence of vitamin B12 and Methionine synthase produces Tetrahydrofolate and Methionine – Due to deficiency of vitamin B12 there is depletion in this process, which causes accumulation of 5-Methyltetrahydrofolate consequently reducing formation of various other folate products required for Thymidylate and Purine affecting DNA synthesis and replication thus hampering maturation erythrocytes (Red Blood Cell) resulting into immature, large and fragile Red blood Cells a picture of Megaloblastic Anaemia a feature of Pernicious Anaemia.
SYMPTOMS OF PERNICIOUS ANAEMIA
As described earlier Pernicious Anaemia is a later stage complication of vitamin B12 deficiency. So the patients of pernicious anaemia shows symptoms of Vitamin B12 deficiency along with general symptoms of anaemia. Typically complicating each other and showing involvement of neurological, Psychological, Gastric, Cardiac, aspects as well.
Weakness, lethargy, general debility, malaise, weight loss.
impaired growth in children delayed puberty Palor, pale face, mucousa and conjunctiva.
Blood teat for Vitamin b12 level and Complete Blood Count (CBC)report is required.
Low Vitamin B12 level and low Heamoglobim parameters pancytopenia with a picture of Megaloblastic Anaemia are suggestive criteria for diagnosis of pernicious anaemia.
HOMEOPATHIC TREATMENT OF PERNICIOUS ANAEMIA
Homeopathic treatment of pernicious anaemia depends upon presenting symptoms which systems are involved and the severity of the condition. it is also important to evaluate whether vitamin B12 deficiency is due to insufficient dietary intake or is secondary to some other pathological condition in body like autoimmune disorders etc. and accordingly the patient should be treated
Supplimenting with Vitamin B12 and increasing food rich in vitamin B12 should be first priority in all the cases to bring back vitamin B12 levels back to normal AS SOON AS POSSIBLE to prevent further damage.
HOMEOPATHIC MEDICINES FOR PERNICIOUS ANAEMIA
Constitutional remedy selection and treatment is recomended for all those who have vitamin B12 deficiency secondary to some other disease condition and not primarily due to imsufficient dietary intake of Vitamin B12.
Few of the Homeopathic remedies which may prove useful varing and depending on cases to case in treatment of pernicious anaemia are listed below
Hemophagocytic Lymphohistiocytosis (HLH) is a type of Cytokine Storm Syndrome caused due to uncontrolled proliferation of morphologically benign Macropages and Lymphocytes secreting copious amount of Inflamatory Cytokines resulting into Hyperinflamation.
PATHOPHYSIOLOGY OF HLH
CAUSES OF HLH
Mutations or Single Neuclotide Polymorphism in certain genes gives rise to HLH it can be germ-line defect or may be acquired. There are other factors as well which may cause secondary HLH(sHLH).
PRIMARY HLH -Primary that is without any other underlying disease in background it is termed as HLH
SECONDARY HLH (sHLH) – HLH secondary to some other primary underlying disease condition or Iatrogenic factors in the backgroung is termed as Secondary HLH or (sHLH)
DISEASES THAT CAUSE SECONDARY HLH (sHLH)
ALL – Acute Lymphocytic Leukemia,
AML – Acute Myeloid Leukemia,
Juvenile Idiopathic Arthritis
Juvenile Kawasaki Disease
SLE – Systemic Lupus Erythematosus
Juvenile/Adult onset Still’s Disease,
RA- Rheumatoid Arthritis
Severe Combined Immunodeficiency
Wiskott – Aldrich Syndrome
Ataxia – Telangiectasia
EBV -Epstein Barr Virus
HIV – Human Immunodeficiency Virus
Certain Bacterias, Fungus and Protozoas
IATROGENIC FACTORS THAT CAUSE SECONDARY HLH (sHLH)
Bone Marrow Transplant
PATHOGENESIS OF HLH
HLH is caused due to genetic mutations that may be germ-line defect or acquired
Mutation in gene responsible for decoding a proyien protein in Cytotoxic T-cells and Natural Killer cells which killes virus infected is one of the known factor causing HLH
Genes that have been identified as contributor to HLH are UNC13D, STX11, RAB27A, STXBP2, LYST, PRF1, SH2D1A, BIRC4, ITK, CD27, MAGT1 any SNP or mutation in above mentioned gene that causes decfect in ability to kill virus infected cells or damaged cells.
As the Cytotoxic T-cells and NK-cells lose their ability to kill cells infected with virus or other damaged cells, due to mutation of above mentioned genes, consequently results into uncontroled proliferation of immune system secreting excess quantity of cytokines causing excessive accumulation of Interleukine 1, Interleukine 6, Tumour Necrosis Factor-Alpha, Tumour Necrosis Factor-gamma, Plasminogen Activating Factor, Ferritin etc.
Now excess of IL1,IL6&TNF-alpha leads to fever
TNF-alpha and TNF-gamma in excessive proportion aslo leads to suppression of Heamtopoesis resulting into Cytopenia and inhibition of Lipoprotein Lipase to stimulate Triglyceride Synthesis.
Excess of Plasminogen Activating Factor and Ferritin secreted by activated macrophages leads to Hyperfibrinolysis.
SIGNS AND SYMPTOMS OF HLH
In 70% cases the onset is below one year of age.
Fever, nausea, vomitting, weakness, debility
Hepatomegaly with fatty infiltration in liver
Elevated Liver Enzymes
Icterus and rashes
Spleenomegaly may also show multiple small granulomas in spleen
Lymphomegaly may also show calcified nodes
Erythrocytopenia- Reduced Red blood cells
Leucocytopenia – Reduced White Blood Cells
Thrombocytopenia – Reduced Platelets
Reduced Serum Albumin
Elevated Ferritin especially in children of above 10000 is very sensitive and specific for HLH, but no so in adults.
Incresase D-Dimer, CRP and ESR
DIAGNOSIS OF HLH
All patient with Hyperferritinaemia combimed with Cytopenia should be suspected for HLH and soon be considered for further investigations without wasting time.
To be clinically corelated with above mentioned sign and symptom of clinical presentation and investigations and bone marrow biopsy as mentioned below
Bone Marrow Aspiration and Imprint may show Hemophagocytosis, Cellular Marrow having Dimorphic Maturation with increased Histiocytes and Megakaryocytes
CBC – reduced RBC, WBC and Platelets
Serrum Ferritin elevated
Liver function Test – liver enzymes elevated
Ultrasonography of whole abdomen – Spleen, Liver and Lymphnodes enlarged
Homeopathic Treatment and Medicines of HLH
Its a life-threatening condition and one should not waste time even in suspected cases and all patient with elevated ferritin along with cytopenia should soon be sent for bone marrow biopsy and other confirmatory supportive tests and be kept under constant medical observation.
Homeopathic prescription for HLH should be strictly derived on basis of symptom similarity basis and the potency of homeopathic medicines and repetition of doses should be as per susceptibiloty of the patient and disease symptom and severity as per homeopathic principles.
Homeopathic Medicines for HLH
Below are few homeopathic medicines that could be theraputically indicated and may proove useful in cases of HLH.
Homeopathic medicines for HLH should be strictly dispensed under guidance and observation of homeopathic physician
Autoimmune Hemolytic Anaemia (AIHA) also called Immunohemolytic Anaemia is an autoimmune condition where in there are antibodies driven against our own Red Blood Cells. Due to which there is excessive destruction of RBC reducing oxygen carrying capacity of blood.
Causes of AIHA
Autoimmune Hemolytic Anaemia (AIHA) is believed to be caused due to genetic predisposition and environmental insults on the genome. Still no specific HLA locus has been found which can be related with AIHA in other words, no Human Leucocyte Antigen association has been established yet.
It can be also be secondary to other Autoimmune diseases, Cancers and Infections as mentioned below
1) Autoimmune diseases
Systemic Lupus Erythematosus (SLE)
Chronic Lymphocytic Leukemia
Other Blood Cancers
Human Immunodeficiency Virus (HIV)
Differentiation of AIHA
Based on optimal temperature required for reaction of autoantibody of IgG class and autologous erythrocytes AIHA can be differentiated into
Warm Autoimmune Hemolytic Anaemia (wAIHA)
Cold Autoimmune Hemolytic Anaemia, further classified into i)Cold Aglutinin Disease (CAD) and ii) Paroxysmal Cold Heamoglobinuria(PCT). These both subtypes can be acute or chronic.
Atypical (DAT- negative, IgM -wAIHA)
Classification of AIHA
Clinically AIHA can be clasified as Primary or Secondary
Primary AIHA – It is also called Idiopathic AIHA has no known underlying causative factor and presents itself with hemolysis as predominant feature and other complaints are secondary to it. This type can either be cold or warm thermal relation to reaction mention in above differentiation.
Secondary AIHA – It is usually associated with some primary underlying disease condition. This type usually shows cold thermal relation in reaction that is Cold Agglutinin Disease Category.
Autoimmune Hemolytic Anaemia characterises itself by presence of Anti-RBC autoantibodies with or without activation of Complement-Cascade causing excessive destruction of Erythrocytes(RBC).
There are many mechanisms involved in pathogenesis of AIHA. It is a complex scenario with many mechanisms involing Autoantibodies, Phagocytosis, Antibody Dependent Cell-Mediated Cytotoxity, B Lymphocutes and T Lymphocytes, T regs, Cytokines, and Complement System.
Auto-antibodies are formed by both tissue and circulating self reactive B-Lymphocytes in co-ordination with T-Helper Lymphocytes.IgG sub-classes IgG1 IgG2 IgG3 and IgG4 are involved in ADCC.
Cytotoxic CD8+ T cells and NK cells opsonize the RBC’s with fc portion of IgG for attracting fc receptors on macrophages thus resulting in destruction of RBC by phagocytosis. Occurs in Spleen and lymphoid organs.
Note- Spleenectomy in most cases doesnt have much effect on the disease as in slpeen the erythrolysis is in very lesser proportion in most AIHA cases.
Activation of Final Components of Complement Cascade (Membrane Attack Complex)- DIRECT LYSIS.
IgM dependent- IgM mediated compliment activation results in direct osmotic lysis of RBC, through sequential activation of Membrane attack complex(MAC), in circulation. Also C3b opsonisation of red blood cells by compliment activation results into extracellular erythrolysis by kufper cells of liver, 10 folds more destruction of RBC if compared to ADCC. IgG1 and IgG3 are also responsible in compliment activation to some degree. Majority of erythrolysis is extravascular especially in liver by kufper cells.
SIGNS AND SYMPTOMS
Symptoms develop gradually over months with presenting symptoms usually proportionate to degree of anaemia
General signs of anaemia depending on degree of anaemia like weakness, lethargy, breathless, etc
signs of Red blood cell destruction.
Spherocytes in RBC morphology
Reticulocytes in Circulation
Jaundice which may be mild to moderate or even severe
DIAGNOSIS of AIHA
HOMEOPATHIC TREATMENT FOR AUTOIMMUNE HEMOLYTIC ANAEMIA (AIHA)
Anaemia can be defined as decreased haemoglobin counts or reduced red blood cell counts or reduced oxygen carrying capacity of blood, due to “loss of” or “abnormality of” red blood cells or haemoglobin.
Normal Heamoglobin Counts
6 months to 5 years of age > 11g/dl
5 years to 12 years of age > 11.5g/dl
12years to 16 years of age > 12g/dl
Adult Females (non-pregnant) > 12g/dl
Adult Females (pregnant) > 11gm/dl
Adult Males > 13g/dl
CAUSES OF ANAEMIA
Excessive Red Blood Cell destruction
Anaemia of Chronic diseases
Autoimmune haemolytic anaemia
Inflamatory bowel diseases
Hypervolemia or water retention due to sodium or other salts.
Genetic hereditary conditions like Thalasemia
Reduced erythropoetin production
Excessive RBC destruction
Impaired RBC production
Certain infections like malaria which causes RBC destruction.
Certain drugs which causes RBC destruction eg. Quinine causes chinchonism.
Bone Marrow lesions and pathologies
CLASSIFICATION OF ANAEMIA
There are many types of anaemias. It can be broadly classified into 7 categories depending upon their causes
Anaemia due to
Impaired or abnormal Erythropoesis
Based on RBC morphology it can be classified into 3 groups
FEW COMMON and RARE TYPES OF ANAEMIA
Iron Deficiency Anaemia
Autoimmune Hemolytic Anaemia
Congenital Dyserythropoetic Anaemia
Anaemia of Prematurity
Erythroblastopenia or Pure Red Cell Aplasia
In children it affects growth in general
Somnolence, Drowziness in day time
Disturbed sleep at night
Pallor, general pale appearance of skin, mucous membranes and eyes.
Dyspnoea on Exertion.
Reduced Immunity, tendency to catch infections and slow recovery and healing.
Cyanosis in severe cases
Low blood pressure
Craving for indigestible things , PICA
Cold clammy extremities
Oedematous swelling of extremities, dependent oedema
Angina or cardiac failure in severe cases
Will impact general growth and repair of all the vital organs and tissue of the body.
HOMEOPATHIC MEDICINES FOR ANAEMIA
Depending upon the cause of anaemia and general constitution of the patient, one of the following medicines may be called for duty by a homeopathic physician.
COVID-19 term is derived from “CO”rona”VI”rus “D”isease 20″19” it is caused due to Novel Coronavirus also known as 2019-nCoV or SARS-CoV-2. It is commonly known as Wuhan Coronavirus or Wuhan Sea Food Market Pneumonia Virus is an enveloped positive sense, single strand, RNA Coronavirus with a neucleocapsid of helical symetry which can infect and spread through human to human transmission causing flu like illness officially termed by WHO as Covid-19 where “Co” represents CORONA, “vi”represents virus, “d” stands for disease and “19” stands for year of first outbreak 2019.
Novel Coronavirus 2019-nCoV or SARS-CoV-2 Classification
Novel Coronavirus belongs to
Phylum -Incertia Sedis
Genus -Beta Corona virus
Sub Genus -Serbecovirus,
Virus -2019nCoV or SARS-CoV-2
Coronavirus strands that affect humans
Coronaviruses infects mammals and birds there are total 7 known strands that infect humans including 2019nCoV, first 2 strands were detected in 1960’s
Human coronavirus 229E (HCoV-229E)
Human coronavirus OC43 (HCoV-OC43)
Human coronavirus NL63 (HCoV-NL63, New Haven coronavirus)
Human coronavirus HKU1
Middle East respiratory syndrome coronavirus (MERS-CoV), previously known as novel coronavirus 2012 and HCoV-EMC.
Novel coronavirus (2019-nCoV). This is the strain that causes COVID-19 disease in humans
The first outbreak of the Novel Coronavirus or 2019nCoV in humans was confirmed and notified to WHO by China on 31/12/2019, when patients from Wuhan province of China were suffering with virus related non specific flu like illness from around 8/12/2019 then later the genome was sequenced to confirm this absolutely new and novel strain of coronavirus 2019-nCoV or SARS-CoV-2
Within three months of first reported case on 8/12/2019 the coronavirus outbreak that had first started from Wuhan in China had now reached more than 66 countries including India, Thailand, Japan, South Korea, Italy, Iran, Germany, Taiwan, Hong Kong, USA, Vietnam, Singapore etc. claiming more than 3100+ deaths of estimated 100000+ infected as on 8/3/2020. The death toll is constantly rising, in subsequent two months that is by 8/6/2020 almost 6.5 million got infected and almost 4lac deaths.
It will take some time to estimate mortality rate but it seems to be around 2%. Old people and people with other pre-existing disease condition are at higher risk of succumbing to death. With increasing death rate rises steeply with upto 50-70% death rate in symptomatic patients above 60 with hypertension or diabetes or other complications.
Most of the initial cases were from Huanan seafood market so epizootic origin is suspected.Outbreak of this particular strain of coronavirus is for the first time, So its new for human immune system. As the time lapses the affected community will start developing certain immunity against it, which will slow down the progress of transmission and epidemic as time lapses. Also with time and better understanding of virus and its epidemic, the health authorities will be more efficient in containing the disease and its epidemic.
There is a split between science community where in a group suggests that it has originated from snake where as other claims that snake cannot be the probable the reservoir and is probably from mammal reservoir mostly the bats as the genome sequencing shows 96% resemblance of bat coronavirus and 2019-nCoV.
It is postulated that homologous recombination of Clad A bat viruses “CoVZC45 and CoVZXC21” with some unknown Beta-CoV may have formed 2019nCoV
Human to human transmission of novel coronavirus was confirmed till mid January And the damage was done till then. The virus had started spreading at pace unmatched by any other disease witnessed in past 100 yrs.
PATHOGENESIS OF COVID-19 or Novel Coronavirus 2019 Infection
Still the pathogenesis is not been clearly understood but data and study results are fast pouring in and now we have some basic understanding about but there are many missing gaps and needs to be understood and filled up soon.
The disease causing agent and its full geneome was sequence in December 2019-January 2020, soon after initial outbreak.It was found that the disease causing agent was a virus which had 70% genomic resemblence to SARS-CoV and 50% genomic resemblence to MERS- CoVand they termed it as Novel Coronavirus 2019 or 2019nCoV or SARS-CoV-2 and disease caused by this virus was termed as COVID-19.
Inoculation of 2019nCoV
From initial studies it seems that 2019nCoV attaches to the receptors of Angiotensin Converting Enzyme 2 (ACE2) through an endocytosis process trigerred with the help of spike protein present on surface envelop of the virus . Which are present good quantity on lymphocytes, macrophages, epithelial linning of respiratory mucosa, lungs alveoli, enodthelium of blood vessels, gastrointestinal tract and are also expressed by vital organ like heart and kidneys, which we see getting affected in this disease.
Multiplication and Spread of 2019nCoV
Virus not only has capability to attach to ACE2 receptors of upper respiratory tract and inoculate the cells but also has capability to actively replicate in upper-respiratory tract tissue which was demonstrated by isolating virus from swabs of upper respiratory tract with presence of Sub-Genomic mRNA (sgRNA) in cells of upper respiratory tract. There is tropism of upper respiratory tract and shedding of virus.
All of the above factors explains us fast and easy transmission of virus even in early stage of disease as compared to SARS-CoV and MERS-CoV.
Virus predominantly infects through upper-respiratory in majority cases and then gradually by 3-4 days it involves lower respiratory tract and then by second week there is wide spread invasion into bloodvessels and major vital organs like heart, kidneys with general viremia.
Immune Reaction Towards 2019nCoV Infection and Its Consequences
Its not only virus that causes damage to system but also the body’s immune response against the virus is causing damage to the body which is observed by excessive production of early proinflamatory mediators like Interlukine 6 (IL6) Tumour Necrosis Factor (TNF) Interlukine 1 (IL1), presence of inflamatory infiltrate in lungs. Reduced blood level of T-Lymphocytes and B-Lymphocytes although direct due to viral attack on these cells but also is attributed to redistritbution by immune respone which is demonstrated by presence of comparative more number of T-cell and B-cells at inflamatory sites.
The Cytokine Storm Postulate
There is much evidence to suggest that the initial immune response driven against virus causes activation of coagulation pathway which results in excessive production of early proinflamatory mediators which accumulate overtime leading to vascular hyperpermeability and micro-coagulations resulting from disturbed procoagulant-anticoagulant axis balance due to overt inflamatory response.
Thrombin, known for its primary role in coagulation by activation of platelets and conversion of fibrinogen to fibrin, also has multiple cellular effects that may enhance inflamatory response through Protinase-Activated Receptors(PARs).
Thrombin production is tightly controlled by negative feedback loops and physiological anti-coagulants like Tissue Pathway Factor Inhibitor, Antithrombin III and Protein 3. Inflamatory process can significantly reduce the concentration of anti-coagulants this deviates the fine balance of axis between procoagulant-anticoagulant balance that causes multiple micro-coagulations disseminated intravascular clots and multiple organ failure.
SIGNS AND SYMPTOMS of COVID-19
It shows symptoms that of severe respiratory tract infection giving rise to pneumonia with some gastrointestinal symptoms like other coronavirus infection, Its symptoms are much related to 2003 SARS Epidemic caused due to SARS-CoV.
Most of the patients remain asymptomatic and never get detected many show mild to moderate symptoms this forms the vast majority.
COVID 19 CLINICAL PRESENTATION
Almost 98% symptomatic cases of 2019-nCoV(Covid-19) infection presents with Fever
Dry Coughing is present in almost 82% of symptomatic cases.
Of all the cases sputum production is seen in 25-30% cases and Hemoptysis in upto 5% of all the cases.
Fatigue is observed in almost 70% cases approaching medical care
Muscle-aches (myalgia) in almost 44% of all the cases.
Headaches in almost 13% of all the cases
Diarrhoea experienced in 10% cases
Vomitting seen in 10% of all the patients
Almost 55% of all the cases will develop shortness of breath after 3-8days of initial general symptoms.
Almost 20% of all the the cases seem to progress into severe disease with respiratory distress symptoms within a day or two of developing shortness of breath.
Few patients go into shock and may develop cardiac arythmias.
Of all the cases less than 5-10%(approx) will die due to complications, mostly those who are elderly children or have other prevailing disease condition like diabetes, cardiac diseases, cancer etc.
X – ray and CT scan shows bilateral Lungs involvement with Ground Glass Opacities, grey white consolidated patches.
Leucopenia -Low WBC count especially lymphocytes – lymphopenia.
Increased Neutrophil to Lymphocytes Ratio(NLR)
Increased D. Dimer
Reduced Prothrombin time
Reduction in bleeding and clotting time.
Window period of 2019-nCoV ranges between 2-14days. It takes 2-14 days for symptoms to appear post exposure to virus. Note the patient of 2019 nCoV (Covid-19) can spread infection to others even during this window period l, that is, even before any symptoms starts appearing after first inoculation of 2019-nCoV into body or even any test to decisively test positive.
After window period is over and the symptoms starts appearing the following pattern is seen in progression of clinical symptoms commonly found in most cases.
DAY 1-2 Initially on first 1-2 days patient will show mild fatigue malaise and heaviness of head with mild rise in temperature, few will show a peculiar symptom of Olfactory loss- loss of taste and smell(usually this type of presentation shows mild disease form and has has good prognosis).
DAY 2-3 Gradually the temperature will increase from 2-3rd day with mild irritation in throat.In many this symptom will stop increasing at this stage and will remain mild symptomatic throughout the course of disease, in rest it will progress with fever exceeding 100F, bodyaches, joint pains, weakness
DAY3-4 Fever continues to relapse with dry cough a very few minority might start showing development of shortness of breath even at this early stage.
DAY4-6 Loose motion is frequently encountered on once or twice between 4th and 6thday(in few minority it has appeared right on day one of initial symptoms) this might bring in weakness and exhaustion in patients and those with high fever may be drained even more by accompanying diarrhoea. Few might go into respiratory distress at this stage.
DAY 7–8 From 7th day onwards in few patients fever starts subsiding a bit but in many it persists and few go into respiratory distress.
DAY 8-9 Now 8th-9th days are important to observe as from here on majority patient’s immune system will develop sufficient immunity and resistance against virus and fight it off from the body and recover. Their fever breaks away and they start feeling better with weakness leaving their body but in few cases there is no recovery at this stage such patients progresses into critical stage either fever continues or breathlessness sets this is when the patient needs be urgently shifted to ICU.
Patients with co-morbidity like Diabetes Mellitus, Cardiovascular or Kidney diseases, Immuno-compromised, Organ failure, Asthma Bronchitis, Chronic Obstructive Pulmonary Disease(COPD),Cancer, Autoimmune diseases, Severe anaemia, etc.
Greater severity of pneumonia at presentation.
Elderly patients – Older the age greater the risk.
Radio-opacities and/or pulmonary infiltrates on X-ray findings
Neutrophil to Lymphocyte ratio (NLR) of more than 3.13
SPO2 level below 95%
Increased BUN or Serum Creatinine
Increased Liver enzymes SGOT SGPT, Bilirubin
Any neurological event
Increased D Dimer
Reduced bleeding time
Reduced Clotting time
Reduced Prothrombin time
Transeminated intravascular clot.
There are two types of testing approach one is direct test and indirect test.
1) DIRECT TEST :-
Throat Swab for RT-PCR for SARS CoV-2
detects viral protein through Polymerase Chain Reaction PCR it is gold standard test as it amplifies/enhances virus protein to detectable levels and give most accurate results possible as we are directly detecting virus. But it is comparatively more costly and time consuming. Still it’s recomended as rapid antibody tests(indirect tests) that are available till date are too inaccurate to rely
2) INDIRECT TEST :-
Blood Test for Antibodies IgM and IgG against SARS CoV-2
Herebwe are not directly detecting the virus but we try to find out antibodies formed against 2019-nCoV/ SRAS CoV-2 virus. It is comparatively rapid in nature but not accurate. Presence of antibodies – IgM and IgG against SARS CoV-2 are indicators of past or active
Interpretation of blood test for diagnosis of Covid 19
RT-PCR -ve, IgM -ve & IgG -ve Means No current, No past infection or may be window period.
RT-PCR +ve, IgM -ve & IgG -ve means early infection no immune response developed
RT-PCR +ve, IgM+ve & IgG -ve suggests infection with early acute phase immune response developed.
RT-PCR +ve, IgM +ve & IgG +ve means later stage of infection with with longer lasting immune response developed.
RT-PCR +ve, IgM -ve & IgG +ve suggests acute phase of infection is recovered and virus is being neutralised and strong immunity is being developed.
RT-PCR -ve, IgM-ve & IgG +ve means infection has completely resolved and there is nonvirus in body and patient is non infectiois and has developed certain immunity towards virus for quite some time.
Time Line of Sensitivity of various Laboratory Investigations for Covid 19.
Day 0: Infected (innoculation)
Upto Day 5: Onset of symptoms(variable 2-21days, with 11.2days average)
Day 7: IgM positive – (from Day 7 toDay 21)
Day 14: IgG positive
Day 21: IgM disappears
Days 1-28: SARS CoV2 RNA & Antigens will be positive
Day 28: SARS CoV2 RNA & Antigens disappears
Disease Progression, Antibodies, Viral load, and Infectivity
Day 0 -Day 7: Window Period, Asymptomatic, Only PCR positive in this Phase, negligible Viral load on day 0-1 but viral load starts increasing very speedily and within a couple of days patient from mildly infectious on day 0 and 1, becomes considerably infectious and infectivity keeps increasing with each passing and in no time patient becomes highly infectious by the end of this period.
Day 7- Day 21: Symptomatic, both PCR and IgM Positive, Patient is highly infectious.
Day 14- Day 21: Decline Phase, PCR, IgM and IgG positive, Patient is highly infectious.
Day 21- Day 28: Convalescence Phase,IgM negative, IgG positive, PCR on declining count, Patient is still infectious.
After day 28: most of the patients are recovered and also PCR turns negative,so they are not infectious, IgG remains elevated,
Chest CT scan along with clinical picture and other blood tests like D.Dimer, CBC, NLR, ABG, CRP and ESR, LDH is also very important tool to give direction in diagnosis especially during pandemic when resources are less for RT-PCR. CT scan pattern may help to establish provisional diagnosis, during pandemic, which later can be confirmed by RT-PCR.
PREVENTION OF NOVEL CORONAVIRUS INFECTION DURING TIMES OF COVID-19 PANDEMIC
COVID 19 is caused by 2019-nCoV also called SARS-CoV-2. It is a highly contagious virus. The virus can spread even through casual contacts and proximity.
Current studies suggests that virus can survive on surfaces like glass, plastic, metals etc for may be up to 9days and in fecal material for may be upto weeks of which studies are still going on for confirmation.
It has spread to infect more than 63,00,000 person worldwide within a very short span of just 5months since its outbreak. Time and again most of the types of Coronavirus have proven themselves to have potential to create global pandemic claiming many lives within no time. Looking at the scale of pandemic and potential of 2019nCoV virus to spread very fast and claim lacs of lives in no time has spread panic and concern throughout the world as fast increase in cases of COVID-19 has overwhelmed the healthcare system even of the best country of the world with doctors finding them helpless against the disease and its scale and so almost all the major countries of the world have implimented partial or complete lockdown and social distancing norms to contain and slow down the spread of virus.
Keep distance from infected person, at least 6 feet of distance is recomended
Wear masks in public places
Avoid traveling to area affected with 2019-nCoV epidemic
Quatrantine patients traveling from COVID-19 epidemic regions.
Avoid contact with person known to have came in contact with any person infected with 2019-nCoV or travel history from affected area.
Report any case of cough, cold, fever or symptoms of flu to health authorities found in all the regions where cases of SARS-CoV-2 also called 2019-nCoV is prevailing.
Person staying in affected regions should stay within their home and avoid any public places as much as possible.
While moving out in affected region, wear removable and easily washable overcoats, wear disposable gloves, protective eye wears.
Touching with bare hands to public handle, buttons, walls curtains and other objects in public places in affected region should be avoided.
When in public place, try to prefer option with open air and lesser crowd then in enclosed public premises.
Dont use public transport unless its unavoidable.
Stay away from sewage channels and fecal material.
Prefer food prepared at home that too fully cooked and avoid uncooked raw food.
Avoid gathering and meeting people during times of epidemic.
Avoid hand shakes and close proximity with other people during epidemic.
Maintain healthy lifestyle and nutrition, food rich in Zinc, Iron and Vitamin C is recomended
Keep all rooms highly ventilated.
Sanitize your hands frequently almost every 1-2hours, wash hands at least for 20seconds at a time.
People with long hairs should keep hair in such a way that it doesn’t come in contact with potentially infected objects in public places e.g. handle on seat back on buses and trains.
Eat nutritious food, daily yoga and exercise sufficient exposure to sunlight, timely meal sleep and exercise helps boost health and immunity to prevent and fight the disease.
When and how to use mask correctly is explained and demonstrated in the video below by WHO
HOMOEOPATHIC MEDICINE ARSENICUM ALBUM 30 PREVENTIVE MEDICINE AGAINST CORONAVIRUS DURING COVID -19 PANDEMIC
Expert committee of MINISTRY OF AYUSH, GOVT OF INDIA has identified Arsenicum Album 30 as Genus Epidemicus for immunity enhancement during COVID-19 pandemic and has recomended issuing public notice regarding the same. It has also recomended registered homeopathic practioners of India to suggest identified COVID-19 Genus Epidemicus Arsenicum Album 30 to people as immunity enhancement during the COVID 19 pandemic.
As per Ministry of Ayush, Govt of India Circular:-
Central Council for research in Homeopathy and Ministry of Ayush on its 64th Scientific Advisory Board meeting date 28th January 2020, recomended that Arsenicum Album 30 could be taken as prophylactic medicine against coronavirus infection in following prescribed dose
One Dose of Arsenicum Album 30 on Empty Stomach For 3 Consecutive Days
The Dose Should Be Repeated After One Month Following The Same Schedule.
Other Precautions that needs to be followed during homeopathic medication
Do not eat or drink anything at least for 1 hour after taking medicine. Plain water or milk at room temperature could be consumed during this one hour if required.
Brush Teeth at least one hour before or after taking this doses i.e one hour interval prior and after the dose.
Avoid Uncooked Onion, Uncooked Garlic and Coffee atleast for 5 days when you start medicines.
Homeopathic Medicines Indicated For COVID-19 Novel Coronavirus Infection
As per my view other than basic symptomatic supportive treatment and available regular conventional allopathic treatment, homeopathic medicines can be used in conjunction, as per indication under guidance and observation of both qualified homeopathic physician and allopathic physician.
Few of the Homeopathic medicines that can be useful in treatment of COVID-19 that is SARS-CoV-2 infection also called 2019 novel coronavirus infection are listed below.
Initial stage of fever or first day of symptoms in patients much fear and anxiety. Also this medicine can be used for patients having psychological problems of fear fright and anxiety due to COVID-19 pandemic and lockdown psychological effects.
This remedy may prove useful for heaviness of head, fever and bodyaches in COVID-19
This is wonderful drug used since ages to treat respiratory complaints be it asthma, allergic rhinitis, viral respiratory infections or bacterial respiratory infections. Arsenic is consumed by mountaineers since ages which helps them to survive in higher altitudes in low oxygen environment it shall work well in any stage of Covid 19 infection. Itcan also be brought into service in patirnt with breathlessness and respiratory distress. Arsenicum Album acts not only on respiratory sphere but also gastrointestinal sphere which should cover the sptom of diarrhoea that many Covid-19 patients present along with respiratory and general symptoms. It should work well in Covid 19 patients with weakness where the patient is mentally restless but physically too weak to move.
USE OF ARSENICUM ALBUM AS HOMEOPATHIC GENUS EPIDEMICUS TO ENHANCE IMMUNITY AGAINST CORONA VIRUS DURING COVID-19 PANDEMIC
ARSENICUM ALBUM 30 is being identified as Genus Epidemicus and is suggested by Ministry of Ayush, Government of India under consultation of Central Council For Research in Homeopathy that it could be taken as prophylactic against Coronavirus infection one dose every morning on empty stomach for three consecutive days and same protocol should be repeated after a month of the epidemic still prevails in the region.
Cytokine-Storm is associated with increased capalilary permeability and disemminated intravascular coagulation due to overproduction of early-proinflamatory cytokines causing imbalance in procoagulant-anticoagulant balance causing microcoagualations in complicated cases of COVID19.
Arnica Montana is commonly used medicine in homeopathy to dissolve internal clots by stimulating body’s natural pathways to dissolve clots and in inverse concentration un-homeopathically it is also used to form clots stop to stop bleeding. So Arnica Montana has both the type of effects procoagulant and anticoagulant depending on what concentartion and repetition its uses. So with correct homeopathically succussed dilution and correct posology it may prove useful in such acute life threatening situation condition of sudden cytokine storm which causes dissemminated intravascular coagulations with damaged leaky hyperpermeable capillaries .
This medicine works well in cases who are living in region where days are hot and nights are cold. dry coughing, shortness of breath, fever, body aches, muscle aches are some of the symptoms covered by bryonia in COVID-19 patients. Master Hahnemann recommends bryonia alba in epidemics during summer season affecting respiratory system.
Camphora made from camphor can be used in terminally ill COVID-19 patient with gross signs of circulatory insufficiency, cyanosis, hypoxia and this should be the first medicine brought in immediately administered in cases of sudden collapse. Typically it has to be used in higher potency as recomended by some homeopaths.
Agaricus muscarius typically used in homeopathy for frosbite and cyanosis of extrimities can prove beneficial in terminally ill COVID-19 patients with signs of cyanosis and bluish discolouration of extremities like finger and toes this homeopathic medicine should be called in for service.
crategus oxyacantha may prove of great service in COVID-19 patients having cardiac complaints and high lipid profile having circulatory distress and disseminated intravascular coagulations crategus should be thought of is complimentary and supportive medicine.
Aspidosperma Quebracho successfully used in homeopthic mother tincture form since ages for treatment of acute exacerbations of asthma and cardiac asthma may prove useful in COVID-19 patients that has cardiac complaint and develop Cardiac Asthma.
Antimonium Tartaricum shall prove useful for COVID-19 patients living in region with high humidity near sea-shores works wonders in relieving rattling cough with thick mucous especially in aged.
Kalium Bichromicum is very commonly used medicine in homeopathy which is helpful in getting rid of thick stringy ropy mucous it may prove of great service in COVID-19 cases with accumulation of thick mucous difficult to bring up.
Justicia Adhatoda also known as Vasaka in indian medicine and iss used in Ayurveda since ages. It is a great expectorant if used in lower potency preferably in homeopathic mother tincture form.
Thalasemia is a genetic disorder where in mutation or deletion in any genes responsible to produce globin chain of haemoglobin results in abnormal haemoglobin production.
Normal adult has Haemoglobin A (HbA). HbA is a hetrotetramer of two α globin chains and two β globin chains. In normal humans there are total 4 genes (2pairs) for production of αglobin chain and 2 genes(1 pair) for production of β globin chain. When there is defect in genes producing α globin or β globin chains of heamoglobin it results into thalasemia.
Alpha Thalasemia – Abnormal or dhieficient α globin chain production
Beta Thalasemia – Abnormal or deficient β globin chain production.
Delta Thalasemia – Abnormal or defective delta chain production.
Thalasemia in combimation with other haemoglobinopathies like – Haemoglobin S , Haemoglobin E, Haemoglobin C, Haemoglobin D.
Of the above all types the most common types alpha and beta are discussed below.
Alpha Thalasemia has defective α globulin chain production. Genes responsible to produce α globin chain are situated on chromosome 16. HBA1 and HBA2 genes are responsible for production of α globin chain. Both the genes are acquired from both the parents so total two HBA1 and two HBA2 genes. So, there are two genes acquired from each parent making total 4 genes or two pairs(αα/αα) responsible to produce α globin chain.
Depending upon number of gene deleted the condition is classified into 4 categories
α Thalasemia Silent (1 gene deletion)
α Thalasemia Trait (2 gene deletion)
HbH disease (3 gene deletion)
Hb Bart Syndrome (all 4 gene deletion)
Alpha Thalasemia Silent
Any one gene deletion (-α/αα), one of the two allele not received from one parent. Usually there are no sign of anaemia as the remaining three genes produce sufficient alpha globin chains. Althought they dont show symptoms they are the silent carrier and if married to person with one or more α globin making gene deletion then some of their offsprings will have symptoms, probability and severity of the disease in the offsprings will depend on number of gene deletion in the partner.
Alpha Thalasemia Trait
Any two gene deletion, it can be of two genotypes as descussed below, this type shows mild anaemia symptoms.
Two gene deletion – homologous; one of the two allele not received from each parent(-α/-α).
Two gene deletion- heterologous; both the alleles not received from one parent (–/αα).
Three gene deletion (–/-α) No copy of gene received from one parent and only one of the two copy received from another parent. These causes very low α chain production resulting into excess proportion of β chains causing formation of unstable haemoglobin tetramer made up of 4 β globin chains, instead of two α and two β. This type of haemoglobin with all 4 globin chain of β globin is called HbH which is very unstable. These individuals shows moderate to severe anaemia and other thalasemia related symptoms.
Hb Bart Syndrome
All four gene deletion (–/– )No copy of α chain producing gene received from either of the parent. It is a fatal condition where in there are no α chains produced and results into severe fetal condition called hydrops fetalis. Death ensues soon after birth.
Beta thalasemia has defective β globin chain production. For production of β globin chain there is only one gene acquired from each parent makin it total one pair(β/β) i.e total 2 genes responsible to produce β globin chain. Gene Responsible for production of β globin chain is called HBB and is located on chromosome 11.
Beta Thalasemia Minor
(b/β) One gene received from a parent is altered and the one from other parent is normal.
(-/β) No gene received from a parent and the gene received from another parent is normal.
Beta Thalasemia Intermedia
(b/-) One copy of gene received from a parent altered and one from another parent is absent.
(b/b) Genes received from both the parent are altered.
Beta Thalasemia Major
(-/-) No genes producing β globin chain received from either parent.
SIGNS AND SYMPTOMS
Symptoms and its severity depends upon the above mentioned severity of genotype the individual has few complaints which patient with this disease condition show are mentioned below.
General growth is slow
Complete blood count
HOMEOPATHIC TREATMENT AND INDICATED HOMEOPATHIC MEDICINES FOR THALASEMIA
LYMPHOMA – Malignant neoplasm of lymphoid tissue is called Lymphoma.
They are type of blood cancers where in there is abmormal cell-proliferation of Lymphoid Tissue.
Lymphomas and Leukemias both fall under a broader category “Malignant Neoplasms of Lymphoid and Heamatopoetic Tissue” or cancer of Lymphocytes”. Wherein unlike Leukemias, the term Lymphomas is precisely restricted only to the Tumours of Lymphoid tissue.
Types of Lymphoma
Non Hodgkin Lymphoma
Epstein Barr Virus Infection
Non Hodgkin’s Lymphoma
Human T-Lymphotropic Virus Infection
Exposure to certain Pesticides
SIGN’s AND SYMPTOM’s
Pel-Ebstein Fever – Intermittent Fever of around 38C lasting for 1-2weeks and relapsing again after days to weeks
Weight loss of more than 10% within 6 months.
Profuse perspiration especially at night.
Anorexia – loss of appetite
Weakness and fatigue
Dyspnoea on slightest exertion
Ann Arbor Staging System
StageI – Single Lymphnode and surrounding area involved
StageII – Two areas involved a lymph node and another area and both are on the same side of daiphram either above or below
StageIII – Affected areas on both the sides of daiphram with one organ or region near lymphnode or spleen
StageIV – Diffused and disseminated with more than one Extra-Lymphatic organ involved incliding Liver, Bone Marrow, nodular involvement of Lungs.
A or B – type symptom – When patient has following three constitutional symptoms then patient is categorised into B-type symptoms 1) Pel-Ebstein Fever. 2) Weight loss and 3)Night Sweats. When there are no above mentioned combination of B-type constitutional symptoms present then patient is categorised into A type.
“S ” – Disease with Slpeen involvement is denoted with S modifier.
” E” – When disease involves extranodal region that is region surrounding the lymphnodes it is denoted with E modifier.
“X” – X is denominated when the largest bulky deposit region is more than 10cm or if more 35% area of chest is occupied by mediastenum on X-Ray.
Nature of Stage
Clinical Staging “C.S.” – C.S. Mentioned when staging is done based on clinical examination and test.
Pathological Staging “P.S.” – When Staging is done based on pathological findings through invasive techniques like surgical excision etc its Mentioned as P.S.
Biopsy of Lymph node to confirm Lymphoma.
Further to classify Lymphoma:
Fluorescence in-situ Hybridisation.
CT scan and PET scans helps us evaluate extent of spread of the condition and its staging.
HOMEOPATHIC MEDICINES FOR HODGKIN’s LYMPHOMA and NON- HODGKIN’s LYMPHOMA
Abnormal proliferation of blood cells due to defective medullary heamatopoetic stem cells is called leukemia.
In Layman terms, defective bone marrow causes uncontrolled multiplication and abnormal growth of cells that are components of blood causing blood cancer.
TYPES AND CLASSIFICATION
Based on speed of progression and maturity level of most cells most of the Leukemia can be categorised into
Acute – Fast progressing takes weeks to few months, Most of the cells are blast cells (immature cells), Requires immediate treatment, Commonly seen in children.
Chronic – Relatively slow progressing takes months to years, has relatively mature cells, patient usually inder observation before commencing any aggressive treatment, Common in elderly people.
There are some leukemia which do not follow fixed pattern also presentation of symptom may vary in different individual and also there are cases where in they change the classical course of and speed of progression.
Based on types of cells involved, most of the Leukemia can be categorised into
Lymphoid (Lymphocytic) – Precursors of Lymphocytes are involved. It is further classified as per which lymphocytes are involved wether B-cells or T-cells.
Myeloid(Non-Lymphocytic) – Precursors of RBC, Non-Lymphocyte WBC and Platelets are involved.
A Lymphoid or Myeloid leukemia can Either Acute or Chronic as described below
Acute – Lymphoblastic(ALL)
Chronic – Lymphocytic (CLL)
Acute – Myeloid (AML)
Chronic – Myeloid (CML)
Acute Lymphoblastic Leukemia (ALL) –
When there are multiple mutations in the locus, that control cell proliferation, cell maturation and cell death of precursor cells of Lymphocytes called Lymphoblast then this results in ALL. ALL can be of T cell type or B cell type.
Genes associated with ALL –
KMT2A – Infant ALL – onset before 10yr of age
PAX5 – Inherant Autosomal Dominant
ETV6 – Inherant Autosomal Dominant
Certain syndromes that increases risk of ALL
Neurofibromatosis Type 1
Paroxysmal Nocturnal Heamoglobinuria
Severa Combined Immunodeficiency
Schwachmann Daimond Syndrome
SUBTYPES OF ALL
Precursor B-cell ALL
Precursor T-cell ALL
Mature B-cell ALL(also called Burkitts Leukemia due to its similarity with Burkitts Lymphoma)
Acute Biphenotypic Leukemia.
Acute Myeloid Leukemia (AML)
It is an acute Non-Lymphocytic type of malignanacy which involves myeloblast cells(precursor of monocytes and granulocytes).
In AML there is mutation of genes that mature and differentiate the myeloblast cell will arrest maturation and differentiation and the cell will freeze in undifferentisted immature state and when this type of mutations combined with mutations in genes controlling proliferation in same cell will result in clonning of immature undifferentiated cells resulting in AML
Genes associated with AML
Subtypes of AML
Subtypes of AML are classified based on staging of maturation i.e. at which stage the msturation of the cell is arrested and how is the general behaviour of cells and which genes are involved.
Undifferentiated Acute Myeloblastic Leukemia
Acute Myeloblastic Leukemia with Minimal Maturation
Acute Myeloblastic Leukemia with Maturation
Acute Pro-Myelocytic Leukemia (APL)
Acute Myelomonocytic Leukemia
Acute Myelomonocytic Leukemia with Eosinophilia
Acute Monocytic Leukemia
Acute Erythroid Leukemia
Acute Megakaryoblastic Leukemia
Adult T-Cell Leukemia
Blast Crisis of CML
Chronic Lymphocytic Leukemia (CLL)
B-cell Pro-Lymphocytic Leukemia(B-PLL)
T-Cell Pro-Lymphocytic Leukemia(T-PLL), T-PLL doesnt completely fit into this category.
Large Granular Lymphocytic Leukemia(LGLL)
Chronic Myeloid Leukemia (CML)
Chronic Granulocytic Leukemia
Chronic Neutrophillic Leukemia
Chronic Myelo-Monocytic Leukemia(CMML)
Atypical CML (aCML)
Chronic Eosinophillic Leukemia
Few other types, preleukemias and syndromes that cannot be classified in above category
Other Myelodysplastic Syndromes
Leukemia is caused due to mutations in genes that are associated with proliferation, differentiation, growth, maturation and cell death of blood cells. With different types of mutations responsible for different types of leukemia.
These genetic mutations can be inherited or acquired due to multiple reasons of which few known risk factors are
Exposure to certain chemicals (e.g. benzene, petrochemicals, hair-dyes, agent orange herbicide, certain insecticides)
Radiation – ionising radiations and doubtedly non-ionising radiations too.
Smoking and tobacco use.
Prior alkylating chemotherapy for some other form of malignancy.
Viruses – Human T-cell Lymphotropic Virus – 1 HTLV-1 is associated with Adult T-cell Leukemia and Hepatitis C is associated with CLL
Diseases and Syndromes – Down’s Syndrome, Kline Felter syndrome, Fanconi Anaemi, Ataxia-Telangiectasia or Louis-Bar Syndrome, Myelodysplastic syndrom, Myeloproliferation syndrome.
Few of these factor are seen responsible for specific type of cancer (eg HTLV1 causes Adult T-cell Leukemia, Tobacco and Down’s Syndrome increases risk of AML).
SIGNS AND SYMPTOMS
Symptoms may vary in different types of leukemia, different individuals and different stages of disease.
Paleness due to anaemia
Shortness of breath
Headache, lethargy, stiffness of neck
Loss of appetite
Tendency to catch infection too frequently
Fever usually due to secondary infections
Painful long bones
(Heamorrhagic diathesis) easily bleeds and frequent ecchymosis and petechiae (bruises).
Painless lymphomegaly (Enlarged lymphnodes)
Hepatospleenomegaly – can easily palpate liver and spleen due to its increased size.
Fibrosis of bone marrow
Chloroma or Leukemia Cutis or myeloid sarcoma or granular sarcoma or extramedullary myeloid tumour
Swollen painfull and bleeding gums
Cranial nerve Paralysis if CNS is involved
Increased blood cell count , WBC or RBC or Platelets, depending on type with most if the cells immature and lacking differentiation.
Complete Blood Count
Bone Marrow Biopsy
Lymph Node Biopsy
HOMEOPATHIC TREATMENT WITH INDICATED HOMEOPATHIC MEDICINES
Mycosis Fungoides is a type of Non-Hogkin Lymphoma. It is the most common type of Cutaneous T-Cell Lymphoma(CTCL).
Mycosis Fungoides is a misnomer which means “Mushroom-like fungal disease” but by no means it is a fungal condition. It is a type of blood cancer caused due to unusual expression of Skin-associated CD4 T-Cells. This cancer affects skin and produces various lesions on skin and rarely metastatise in other tissues.
It is a fatal condition with 10year survival rate of less than 70% which is even less in elderly.
It usually appears in people above 20years of age and is more common after age of 50yrs , males are affected more than females, the disease tends to be more fatal in black race. Survival rate has been found good in married white women.
Causes of Mycosis Fungoides remains unclear
No hereditary or genetic factors have been found associated to the disease.
It is considered to be non-contagious but some studies suggest that Human T-cell Lymphotropic Virus is associated with this condition.
Initially disease shows symptoms that are not distinguishing and in most of the cases it resembles psoriasis or eczema. Even on biopsy it can not be diagnosed easily in early stages. Even in later stages multiple biopies are required to establish diagnosis.
Disease presentation begins from skin as exfoliating, pruritic, erythodermic eruptions resembling to Eczema or Psoriasis and is almost always mistaken initially in most cases. These eruptions tends to appear first on buttocks in vast majority of cases and then spreads throughout the body. Pruritus is present in only 20% of all the cases. In later stages tumourous and ulcerative lesions may also appear. Disease usually in most cases starts appearing at around age of 45-50 and is a slow prohressing condition with and its usually around age of 60+ that mist patient starts presenting symptoms of later stages like tumours, generalised pruritus and erythrodrema and ulceration. Though in many cases it may start as early as age of 20 and rarely before 20yrs of age. The diseases is classified into three stages
Stages of Mycosis Fungoides
Mycosis fungoides is divided into three stages viz.
Pre Mycotic Stage
It starts appearing on skin at this stage as erythematous, pruritic, exfoliating skin eruptions.
On biopsy it cannot be diagnosed at this stage as histopsthology shows pattern of non specific dermatosis with epidermal psoriasiform changes.
In Mycotic stage Infiltrative Plaques starts appearing as slightly raises or wrinkled spots.
On histopathology polymorphs and few atypical lymphoid cells are seen inflamatory infiltrates in dermis. When this cells are seen lined up.in epidermal basal layer without spongiosis then its confirmatory finding to establish diagnosis of mycosis fungoides.
Nodular overgrowths are seen on skin ranging from few milimeters to centimeters scattered throughout the body along with plaques and patches. Usually it appears on the same place where the plaques and patches are. Also there is erosion of the tumours and ulcerations is seen in many cases over the tumour and plaques.
On histopathology they show medium sized lymphocytes with cerebroid nuclei expands dermis.
DIAGNOSIS OF MYCOSIS FUNGOIDES
Diagnosis is based primarily on histopathological findings of the skin lesions
Clinically patients showing features suggestive of or doubted mycosis fungoides are closely monitored over the time untill biopsy confirms. Multiple boipsies of various lesions might be required at every progressing stage untill confirmed, as its very difficult to estsblish diagnosis in initial stafe wether clinically or histopathologically as it resembles psoriasis or eczema.
On histopathology following findings are required to establish diagnosis of mycosis fungoides
Band-like lymphocyte infiltrate in superficial papillary dermis
Cerebroid T-cells in dermal and epidermal infiltrate
Pautriers Microabscesses – though not present in most cases but is characteristic finding of mycosis fungoides where in the epidermal infiltrate shows atypical lymphocytes arranged in aggregates of four or more.